Kaixin San-medicated serum attenuates Aβ_(25-35)-induced injury in SH-SY5Y cells by regulating autophagy.
10.19540/j.cnki.cjcmm.20241012.401
- Author:
Han-Wen XING
1
;
Yi YANG
1
;
Yan-Ping YIN
1
;
Lan XIE
1
;
Fang FANG
1
Author Information
1. School of Chinese Materia Medica, Beijing University of Chinese Medicine Beijing 102488, China.
- Publication Type:Journal Article
- Keywords:
Akt/mTOR;
Alzheimer′s disease;
Kaixin San;
autophagy;
medicated serum;
neuroprotection
- MeSH:
Humans;
Autophagy/drug effects*;
TOR Serine-Threonine Kinases/genetics*;
Amyloid beta-Peptides/toxicity*;
Proto-Oncogene Proteins c-akt/genetics*;
Drugs, Chinese Herbal/pharmacology*;
Cell Line, Tumor;
Cell Survival/drug effects*;
Peptide Fragments/toxicity*;
Microtubule-Associated Proteins/genetics*
- From:
China Journal of Chinese Materia Medica
2025;50(2):313-321
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this study is to investigate the regulation of Kaixin San-medicated serum(KXS-MS) on autophagy induced by Aβ_(25-35) in SH-SY5Y cells. The SH-SY5Y cell model of Aβ_(25-35)(25 μmol·L~(-1))-induced injury was established, and different concentrations of KXS-MS were added into the culture media of cells, which were then incubated for 24 h. Cell viability was measured by the methyl thiazolyl tetrazolium(MTT) assay. The protein levels of microtubule-associated protein 1 light chain 3(LC3)Ⅰ, LC3Ⅱ, protein kinase B(Akt), p-Akt, mammalian target of rapamycin(mTOR), and p-mTOR were assessed by Western blot. Furthermore, the combination of rapamycin(Rapa)/3-methyladenine(3-MA) and low concentration of KXS-MS was added to the culture medium of SH-SY5Y cells injured by Aβ_(25-35), and the cell viability and the expression levels of the above proteins were determined. The results showed that Aβ_(25-35) decreased the cell viability, up-regulated the expression levels of LC3Ⅱ and LC3Ⅱ/LC3Ⅰ, and down-regulated the expression levels of p-Akt, p-mTOR, p-Akt/Akt, and p-mTOR/mTOR. Compared with the Aβ_(25-35) model group, KXS-MS treatment attenuated Aβ_(25-35)-induced injury and enhanced the survival of SH-SY5Y cells. Meanwhile, KXS-MS down-regulated the LC3Ⅱ/LC3Ⅰ level and up-regulated the p-Akt/Akt and p-mTOR/mTOR levels. Compared with the low-concentration KXS-MS group, Rapa did not affect the cell survival and the levels of p-Akt and p-Akt/Akt, while it up-regulated the levels of LC3Ⅱ and LC3Ⅱ/LC3Ⅰ and down-regulated the levels of p-mTOR and p-mTOR/mTOR. 3-MA significantly reduced the cell survival rate and p-Akt, p-Akt/Akt level in the KXS-MS group, while it had no significant effect on the levels of LC3Ⅱ, LC3Ⅱ/LC3Ⅰ, p-mTOR, and p-mTOR/mTOR. The above results indicate that KXS-MS exhibits protective effects against Aβ_(25-35)-induced damage in SH-SY5Y cells by up-regulating Akt/mTOR activity to inhibit autophagy.
